Syncope

Etiology

Syncope is a symptom of an underlying disease process rather than a disease itself. Although syncope mimics a death-like experience eliciting extreme consternation among both patients and their families, most syncopal events have a benign cause.  Benign causes of syncope reflect vasovagal (also known as neurocardiogenic), volume depletion, or medication-related etiologies. More ominous causes are related to dysrhythmia and valvular abnormalities such as ventricular tachycardia, atrioventricular (AV) block, or critical aortic stenosis. A history of left ventricular dysfunction (with concomitant degeneration of the conduction system leading toward a propensity for dysrhythmias) has been found to be the most ominous predictor of an adverse etiology of a syncopal event.

Causes of Syncope

1. Cardiovascular disorders

• Cardiac arrhythmias (both tachy and bradyarrhythmias)
• Structural and obstructive disorders (valvular abnormalities, HOCM, MI, PE)

2. Cerebrovascular causes (vertebrobasilar insufficiency)

3. Disorders of blood flow and vascular tone

• Vasovagal (neurocardiogenic)
• Orthostatic hypotension (medications, autonomic failure, peripheral neuropathy, decreased blood flow)
• Situational (cough, micturition, defecation, postprandial, deglutition)
• Carotid sinus syncope

4. Others that mimic syncope

• Seizures
• Metabolic (hypoglycemia, hypoxia, symptomatic anemia)
• Psychogenic (panic attacks)

Vasovagal Syncope (Neurocardiogenic syncope, Common faint)

This accounts for almost 50% of all cases of syncope. When faced with certain situations like prolonged standing, crowded places, hot environment, severe pain, extreme fatigue and stress leads to vasodilatation (sympathetic withdrawal) and bradycardia (parasympathetic activity). This condition is also called common faint as it is the common cause of syncope and can occur even in normal people. Syncope events are preceded by prodromal symptoms like blurred vision, diaphoresis, nausea, dizziness, weakness, and then leads to bradycardia, decreased blood pressure, and then lose consciousness. Patients appear pale to the onlookers. Patients normally regain consciousness in few minutes and may experience generalized weakness. They do not lose sphincter control, rarely have any tonic-clonic activity or confusion after regaining consciousness as in patients with seizures. 

Epidemiology

Syncope accounts for around 1 to 3.5% of visits to emergency department visits in the US. Syncope is more common in older patients due to multiple comorbidities and multiple medications. Cardiac etiology is more common in older patients and noncardiac etiology (vasovagal) common in young adults. There is no significant difference in incidence between men and women.

Pathophysiology

The brain needs a constant supply of glucose (through adequate cerebral blood flow) to function and any interruption to this even for few seconds can lead to loss of consciousness or syncope. Cerebral blood flow is maintained by a complex mechanism involving cardiac output, systemic vascular resistance, mean arterial pressure, and intravascular volume. Any defect in one or more of these systems leads to decreased cerebral blood flow. Approximately three-fourths of blood is in the venous bed and any interference in venous return can lead to decreased cardiac output.

Any episode lasting more than a few minutes is not syncope and is more likely to be related to a seizure or other acute neurologic process. Seizures are the most common disease misdiagnosed as syncope. When symptoms overlap too closely, the only way to differentiate seizure from syncope may be with an EEG.

Terms near syncope or presyncope are confusing in that they may convey a different meaning to different practitioners. However, when a practitioner defines near syncope as “a feeling that you were going to pass out but did not” then, near syncope and syncope are both thought to be related to cerebral hypoperfusion, and therefore, any disease process which decreases blood flow can cause syncope and near syncope. 

History and Physical

A thorough history and physical examination alone may yield a diagnosis in up to 50% of patients presenting with syncope. History of syncope should focus on duration, preceding events or precipitating events, and post-event findings.  The position of the patient at the time of the event is important. Syncope in a standing position can suggest vasovagal and in a supine position can be due to neurocardiac causes. A detailed history of the patient's medical problems and medications must be included. The physical examination in syncope should center around vital sign abnormalities as these can often suggest underlying disease processes such as orthostatic hypotension or cardiovascular compromise. Detailed cardiovascular and neurologic examinations should be included looking for signs of vascular disease, congestive heart failure, or an acute cerebrovascular event masquerading as syncope.

Evaluation

Testing rarely leads to a diagnosis as the most common cause is vasovagal and benign. A thorough physical examination is the most important diagnostic tool as it helps in diagnosing the cause and excluding potential life-threatening causes. Choice of diagnostic studies depends on history and physical examination.

In patients presenting to the Emergency department, routine blood work to include hemoglobin, electrolytes, and glucose is indicated. At the minimum ECG is needed in all patients presenting with syncope.

If cardiovascular etiology suspected, further workup includes cardiac enzymes, continuous cardiac monitoring, and echocardiogram. Holter monitor recommended for outpatients suspected of conduction abnormalities.

If cerebrovascular etiology suspected, further workup includes CT head, carotid Doppler ultrasound, MRI brain, and MRA.

Electroencephalography (EEG) indicated if seizures suspected. 

A tilt table test is indicated in:

• Patients with recurrent episodes of syncope of unknown etiology in the absence of cardiac disease. 
• Suspected vasovagal syncope but not sure
• Differentiate between suspected reflex syncope and orthostatic hypotension syncope.

The ECG is the most useful diagnostic study, yielding an etiology of syncope in approximately 5% of patients, while routine blood work leads to a diagnosis in only about 2% of cases. Despite widespread and often indiscriminate testing, approximately 45% of patients will leave the emergency department without a diagnosis following their syncopal event. Recent data suggests that a focused management plan may help diagnose an etiology of the syncopal event and reduce the number of patients discharged without a diagnosis. For example, echocardiography before discharge may be useful in uncovering valvular disease in a patient presenting with a murmur and syncope. Similarly, overnight telemetry or discharge with an event monitor may help expose a dysrhythmia in a patient with evidence of conduction disease on their presenting ECG.[1][2]

Treatment / Management

Treatment of underlying cause is the focus of treatment in syncope. During acute an acute episode, patients should be made to sit or lay down quickly and raising the legs help recovery in patients with reflex postural hypotension event. Placing patients in a horizontal position after the acute event and preventing rising too soon. Treatment of any injuries sustained during a sudden fall from syncope warrants immediate attention.

1. Vasovagal syncope: 

• Conservative measure includes avoiding situations or stimuli that have caused them, Tilt training and increasing use of salt and fluid.
• Drug therapy with beta-blockers, SSRIs, hydrofludrocortisone, proamatine, and few other medications might be useful if conservative measures fail.

2. Orthostatic hypotension:

• Rising slowly from supine and sitting position, a gradual change in posture.
• Avoiding medications that can cause orthostatic hypotension (diuretics, vasodilators).
• Use of compression stocking to improve venous return.
• Intravenous fluids in patients who are intravascularly volume depleted.
• Use proamatine in refractory cases.

3. Cardiovascular disorders: Treating underlying condition by Cardiology. 

Disposition is often the most difficult task in caring for emergency department patients with syncope. Admission rates vary in patients presenting with syncope. In the United States, about 80% of patients presenting to the emergency department following a syncopal event will be admitted. In Canada and elsewhere, admission rates may be as low as 10%. Rather than reflecting differences in acuity, this discrepancy more likely reflects thresholds for missing rare, potentially clinically relevant causes. Practitioners have published multiple pathways with which to risk-stratify syncope patients to help improve this discrepancy; however, all of them appear comparable to a thorough history and examination. The Boston Syncope Criteria center on risk stratifying patients for admission based on prior history of cardiac disease (left ventricular dysfunction, dysrhythmia or valvular disease); concomitant complaints in emergency department presentations of potential cardiac disease such as associated chest pain, dyspnea, or palpations; ECG abnormalities such as signs of ischemia, dysrhythmia, or conduction disease. These criteria suggest that any patient without associated comorbidities and unrevealing emergency department workup should be safe for discharge.

Costs of evaluating syncope have grown exponentially in recent years. Approximately $ 2 billion is spent in the US on patients hospitalized for syncope. [3](B2)

Follow-up: Patients with unknown etiology and without underlying heart disease have a good outcome. Patients with syncope and underlying heart disease needs regular follow-up with a primary care physician and cardiologist. 

Differential Diagnosis

Important differential diagnosis for syncope include

1. Seizure disorder: Seizures associated with aura, tonic-clonic activity, prolonged duration of unconsciousness, urinary and/or bowel incontinence, tongue biting and confusion after regaining consciousness. These differentiate syncope from seizures.

2. Hypoglycemia.

3. Panic attacks: Feeling impending doom, palpitations, air hunger and tingling of perioral region and tips of fingers.

Prognosis

Prognosis depends upon the underlying cause, so identification of the cause is very important. The annual mortality rate can range from 0 to 12% in patients with noncardiac cause and 18 to 33% in patients with a cardiac cause. [4]

Complications

Patients can sustain injuries from fall due to syncope. These injuries can be worse if they were driving during the event.